BACKGROUND: Microglial cells, major immune effector cells in the central nervous system, become activated in neurodegenerative disorders. Activated microglial cells produce proinflammatory mediators such as nitric oxide (NO), tumor necrosis factor-alpha and interleukin-1beta(IL-1beta). These proinflammatory mediators have been shown to be significantly increased in the neurodegenerative disorders such as Alzhimer's disease and Pakinson's disease. It was known that one of the neurodegeneration source is stress and it is important to elucidate mechanisms of the stress response for understanding the stress-related disorders and developing improved treatments. Because one of the neuropeptide which plays a main role in regulating the stress response is corticotropin- releasing hormone (CRH), we analyzed the regulation of NO release by CRH in BV2 murine microglial cell as macrophage in the brain. METHODS: First, we tested the CRH receptor expression in the mRNA levels by RT-PCR. To test the regulation of NO release by CRH, cells were treated with CRH and then NO release was measured by Griess reagent assay. RESULTS: Our study demonstrated that CRH receptor 1 was expressed in BV2 murine microglial cells and CRH treatment enhanced NO production. Furthermore, additive effects of lipopolysaccaride (LPS) and CRH were confirmed in NO production time dependantly. CONCLUSION: Taken together, these data indicated that CRH is an important mediator to regulate NO release on microglial cells in the brain during stress.
Brain ; Central Nervous System ; Corticotropin-Releasing Hormone* ; Macrophages ; Neurodegenerative Diseases ; Neuropeptides ; Nitric Oxide* ; Receptors, Corticotropin-Releasing Hormone ; RNA, Messenger ; Tumor Necrosis Factor-alpha

No abstract available.
Adenocarcinoma ; Cerebral Infarction ; Pancreatic Neoplasms ; Stroke ; Thrombophilia

The object of this study is to measure the transit time and passage rate of capsule endoscopy (CE) in the gastrointestinal tract in medium sized beagle dogs (7~13 kg). Animals were divided into four groups: only capsule (group 1, n=10), capsule+water (group 2, n=10), mettoclopramide+capsule (group 3, n=10), metoclopramide +capsule+water (group 4, n=10). The capsule transit times through the stomach and small bowel were evaluated by radiography findings. Gastric transit time (GTT), small intestinal transit time (SITT) and complete passage rate were measured in four groups. GTT's for each group were as follows; 45+/-20 min (group 1), 117+/-35 min (group 2), 150+/-40 min (group 3), and 154+/-65 min (group 4), while SITT's were 75+/-20 min (group 1), 195+/-55 min (group 2), 70+/-15 min (group 3), and 76+/-15 min (group 4). The complete passage rates were 20% (group 1), 40% (group 2), 20% (group 3), 50% (group 4). In all groups, if CE could pass through the pylorus, it passed all small intestinal tracts within 8 hours (battery life). Administration of water helped CE to pass pylori, except in case of metoclopramide administration. These results indicate that CE could be an useful tool for examining gastrointestinal diseases in the veterinary medicine.
Animals ; Capsule Endoscopy ; Dogs ; Gastrointestinal Diseases ; Gastrointestinal Tract ; Gastrointestinal Transit ; Metoclopramide ; Pylorus ; Stomach ; Veterinary Medicine ; Water

BACKGROUND: Antimicrobial resistance is considered as the primary reason for eradication failure of Helicobacter pylori. Resistance to clarithromycin is mostly due to the point mutation in H. pylori 23S rRNA gene. The aims of this study were to determine the primary resistance rate to clarithromycin and metronidazole and to examine the mechanism of clarithromycin resistance in H. pylori isolates. METHODS: Seventy-nine strains were isolated from 73 patients within about five years. The susceptibility of H. pylori isolates to clarithromycin and metronidazole were tested by E-test and broth dilution test. To detect point mutations in the 23S rRNA gene, PCR-RFLP (restriction fragment length polymorphism) was performed. Mutations in clarithromycin-resistant strains also were analyzed by direct sequencing. RESULTS: The resistance rate to clarithromycin (>1 mg/L) and metronidazole (>8 mg/L) were 5.1% and 54.4%, respectively. Annual metronidazole-resistant rates were 43.7% (7/16) in 1996-1997, 61.1% (11/18) in 1998, 55.6% (5/9) in 1999, and 55.6% (20/36) in 2000. Annual clarithromycin- resistant rates were 6.3% (1/16) in 1996-1997, 0% (0/18) in 1998, 11.1% (1/9) in 1999, and 5.6% (2/36) in 2000. Two of 4 clarithromycin-resistant isolates contained the A2144G mutation. One isolate contained A2143G mutation. One isolate possibly contained T2183C mutation. Different strains, isolated separately from antrum and body in 6 patients, showed same susceptibility to clarithromycin. However, different strains in two patients showed different susceptibility to metronidazole. CONCLUSION: No significant increase of resistantce rate to both clarithromycin and metronidazole were found within recent five years. Resistance of H. pylori to clarithromycin was caused by A2144G and A2143G mutation mainly and by T2183C mutation possibly.
Clarithromycin* ; Genes, rRNA ; Helicobacter pylori* ; Helicobacter* ; Humans ; Metronidazole ; Point Mutation

Here, percutaneous spinal cord injury (SCI) methods using a balloon catheter in adult rats are described. A balloon catheter was inserted into the epidural space through the lumbosacral junction and then inflated between T9-T10 for 10min under fluoroscopic guidance. Animals were divided into three groups with respect to inflation volume: 20 microL (n = 18), 50 microL (n = 18) and control (Fogarty catheter inserted but not inflated; n = 10). Neurological assessments were then made based on BBB score, magnetic resonance imaging and histopathology. Both inflation volumes produced complete paralysis. Gradual recovery of motor function occurred when 20 microL was used, but not after 50 microL was applied. In the 50 microL group, all gray and white matter was lost from the center of the lesion. In addition, supramaximal damage was noted, which likely prevented spontaneous recovery. This percutaneous spinal cord compression injury model is simple, rapid with high reproducibility and the potential to serve as a useful tool for investigation of pathophysiology and possible protective treatments of SCI in vivo.
Animals ; Balloon Embolectomy/*methods ; Disease Models, Animal ; Male ; Rats ; Rats, Sprague-Dawley ; Spinal Cord Compression/*therapy

We induced percutaneous spinal cord injuries (SCI) using a balloon catheter in 45 rats and transplanted human umbilical cord blood derived mesenchymal stem cells (hUCB-MSCs) at the injury site. Locomotor function was significantly improved in hUCB-MSCs transplanted groups. Quantitative ELISA of extract from entire injured spinal cord showed increased expression of brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF) and neurotrophin-3 (NT-3). Our results show that treatment of SCI with hUCB-MSCs can improve locomotor functions, and suggest that increased levels of BDNF, NGF and NT-3 in the injured spinal cord were the main therapeutic effect.
Animals ; Brain-Derived Neurotrophic Factor/*genetics ; *Cord Blood Stem Cell Transplantation ; Enzyme-Linked Immunosorbent Assay ; Gene Expression Profiling ; *Gene Expression Regulation ; Humans ; Locomotion ; Nerve Growth Factor/genetics ; Rats ; Spinal Cord Injuries/*therapy

The use of human umbilical cord blood-derived mesenchymal stem cells for cell transplantation therapy holds great promise for repairing spinal cord injury. Here we report the first clinical trial transplantation of human umbilical cord (hUCB)-derived mesenchymal stem cells (MSCs) into the spinal cord of a dog suspected to have fibrocartilaginous embolic myelopathy (FCEM) and that experienced a loss of deep pain sensation. Locomotor functions improved following transplantation in a dog. Based on our findings, we suggest that transplantation of hUCB-derived MSCs will have beneficial therapeutic effects on FCEM patients lacking deep pain sensation.
Animals ; Cartilage Diseases/etiology/therapy/*veterinary ; *Cord Blood Stem Cell Transplantation/veterinary ; Dog Diseases/etiology/*therapy ; Dogs ; Embolism/etiology/therapy/*veterinary ; Female ; Humans ; Mesenchymal Stromal Cells/cytology/*metabolism ; Spinal Cord Diseases/etiology/therapy/*veterinary ; Treatment Outcome